By Nick Lavars
Keeping ourselves upright is something most of us shouldn't need to think a whole lot about, given we've been doing it almost our entire lives. But when it comes to dealing with more precarious terrain, like walking on ice or some sort of tight rope, you might think some pretty significant concentration is required. But researchers have found that even in our moments of great instability, our subconsciousness is largely responsible for keeping us from landing on our backsides. This is due to what scientists are describing as a mini-brain, a newly mapped bunch of neurons in the spinal cord which processes sensory information and could lead to new treatment for ailing motor skills and balance.
"How the brain creates a sensory percept and turns it into an action is one of the central questions in neuroscience," says Martin Goulding, senior author of the research paper and professor at the Salk Institute. "Our work is offering a really robust view of neural pathways and processes that underlie the control of movement and how the body senses its environment. We’re at the beginning of a real sea change in the field, which is tremendously exciting.”
The work of Goulding and his team focuses on how the body processes light touch, in particular the sensors in our feet that detect changes in the surface underfoot and trigger a reaction from the body.
"Our study opens what was essentially a black box, as up until now we didn’t know how these signals are encoded or processed in the spinal cord," says Goulding. "Moreover, it was unclear how this touch information was merged with other sensory information to control movement and posture."

By Lenny Bernstein
Parkinson's Disease patients secretly treated with a placebo instead of their regular medication performed better when told they were receiving a more expensive version of the "drug," researchers reported Wednesday in an unprecedented study that involved real patients.
The research shows that the well-documented "placebo effect" -- actual symptom relief brought about by a sham treatment or medication -- can be enhanced by adding information about cost, according to the lead author of the study. It is the first time that concept has been demonstrated using people with a real illness, in this case Parkinson's, a progressive neurological disease that has no cure, according to an expert not involved in the study.
"The potentially large benefit of placebo, with or without price manipulations, is waiting to be untapped for patients with [Parkinson's Disease], as well as those with other neurologic and medical diseases," the authors wrote in a study published online Wednesday in the journal Neurology.
But deceiving actual patients in a research study raised ethical questions about violating the trust involved in a doctor-patient relationship. Most studies in which researchers conceal their true aims or other information from subjects are conducted with healthy volunteers. This one was subjected to a lengthy review before it was allowed to proceed, and, in an editorial that accompanied the article, two other physicians wrote that "the authors do not mention whether there was any possible effect (reduction) on trust in doctors or on willingness to engage in future clinical research."

By Peter Holley
"Lynchian," according to David Foster Wallace, "refers to a particular kind of irony where the very macabre and the very mundane combine in such a way as to reveal the former's perpetual containment within the latter."
Perhaps no other word better describes the onetime fate of Martin Pistorius, a South African man who spent more than a decade trapped inside his own body involuntarily watching "Barney" reruns day after day.
"I cannot even express to you how much I hated Barney," Martin told NPR during the first episode of a new program on human behavior, "Invisibilia."
The rest of the world thought Pistorius was a vegetable, according to NPR. Doctors had told his family as much after he'd fallen into a mysterious coma as a healthy 12-year-old before emerging several years later completely paralyzed, unable to communicate with the outside world. The nightmarish condition, which can be caused by stroke or an overdose of medication, is known as "total locked-in syndrome," and it has no cure, according to the National Institute of Neurological Disorders and Stroke.
In a first-person account for the Daily Mail, Pistorius described the period after he slipped into a coma:
I was completely unresponsive. I was in a virtual coma but the doctors couldn’t diagnose what had caused it.
When he finally did awaken in the early 1990s, around the age of 14 or 15, Pistorius emerged in a dreary fog as his mind gradually rebooted itself.

|William Mullen, Tribune reporter
Researchers at Northwestern University say they have discovered a common cause behind the mysterious and deadly affliction of amyotrophic lateral sclerosis, or Lou Gehrig's disease, that could open the door to an effective treatment.
Dr. Teepu Siddique, a neuroscientist with Northwestern's Feinberg School of Medicine whose pioneering work on ALS over more than a quarter-century fueled the research team's work, said the key to the breakthrough is the discovery of an underlying disease process for all types of ALS.
The discovery provides an opening to finding treatments for ALS and could also pay dividends by showing the way to treatments for other, more common neurodegenerative diseases such as Alzheimer's, dementia and Parkinson's, Siddique said.
The Northwestern team identified the breakdown of cellular recycling systems in the neurons of the spinal cord and brain of ALS patients that results in the nervous system slowly losing its ability to carry brain signals to the body's muscular system.
Without those signals, patients gradually are deprived of the ability to move, talk, swallow and breathe.
"This is the first time we could connect (ALS) to a clear-cut biomedical mechanism," Siddique said. "It has really made the direction we have to take very clear and sharp. We can now test for drugs that would regulate this protein pathway or optimize it, so it functions as it should in a normal state."

Injections of a new drug may partially relieve paralyzing spinal cord injuries, based on indications from a study in rats, which was partly funded by the National Institutes of Health.
The results demonstrate how fundamental laboratory research may lead to new therapies.
“We’re very excited at the possibility that millions of people could, one day, regain movements lost during spinal cord injuries,” said Jerry Silver, Ph.D., professor of neurosciences, Case Western Reserve University School of Medicine, Cleveland, and a senior investigator of the study published in Nature.
Every year, tens of thousands of people are paralyzed by spinal cord injuries. The injuries crush and sever the long axons of spinal cord nerve cells, blocking communication between the brain and the body and resulting in paralysis below the injury.
On a hunch, Bradley Lang, Ph.D., the lead author of the study and a graduate student in Dr. Silver’s lab, came up with the idea of designing a drug that would help axons regenerate without having to touch the healing spinal cord, as current treatments may require.
“Originally this was just a side project we brainstormed in the lab,” said Dr. Lang.
After spinal cord injury, axons try to cross the injury site and reconnect with other cells but are stymied by scarring that forms after the injury. Previous studies suggested their movements are blocked when the protein tyrosine phosphatase sigma (PTP sigma), an enzyme found in axons, interacts with chondroitin sulfate proteoglycans, a class of sugary proteins that fill the scars.